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Results for "

cisplatin-induced ototoxicity

" in MedChemExpress (MCE) Product Catalog:

4

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2

Peptides

1

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-128895
    KL1333
    1 Publications Verification

    Quinone Reductase Mitochondrial Metabolism Metabolic Disease
    KL1333, a derivative of β-lapachone, is an orally available NAD+ modulator. KL1333 reacts with NAD(P)H:quinone oxidoreductase 1 (NQO1) as a substrate, resulting in increases in intracellular NAD+ levels via NADH oxidation. KL1333 improves energy metabolism and mitochondrial dysfunction in MELAS fibroblasts. KL1333 protects against Cisplatin-induced ototoxicity in mouse cochlear cultures .
    KL1333
  • HY-N4102

    Apoptosis JNK FOXO Reactive Oxygen Species (ROS) Caspase Neurological Disease
    5,7-Dihydroxy-4-methylcoumarin is an antioxidant. 5,7-Dihydroxy-4-methylcoumarin protects mouse cochlear hair cells from Cisplatin-induced damage, enhances cell viability and inhibits apoptosis. 5,7-Dihydroxy-4-methylcoumarin downregulates phosphorylated JNK levels, increases the ratio of phosphorylated FoxO1 to total FoxO1, scavenges free radicals, reduces ROS accumulation, maintains mitochondrial membrane potential and alleviates mitochondrial dysfunction. 5,7-Dihydroxy-4-methylcoumarin downregulates the expression of caspase-3 and improves cell viability. 5,7-Dihydroxy-4-methylcoumarin can be used in studies related to ototoxicity .
    5,7-Dihydroxy-4-methylcoumarin
  • HY-B0639C

    WR2721 sodium

    MDM-2/p53 HIF/HIF Prolyl-Hydroxylase Neurological Disease
    Amifostine sodium (WR2721 sodium) is a phosphorus sulfate with radioprotective activity. Amifostine sodium can cause splenic vasodilation and may block autonomic ganglia. Amifostine sodium is clinically used to prevent cisplatin-induced ototoxicity .
    Amifostine sodium
  • HY-128895A

    Mitochondrial Metabolism Quinone Reductase Metabolic Disease
    KL1333 hydrochloride is an orally active NAD + modulator that reacts with NAD(P)H:quinone oxidoreductase 1 (NQO1) as a substrate, leading to increased intracellular NAD + levels through NADH oxidation. Elevated NAD + levels trigger activation of SIRT1 and AMPK, and subsequently activate PGC-1α. KL1333 hydrochloride improves energy metabolism and mitochondrial dysfunction in mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) fibroblasts. KL1333 hydrochloride protects against cisplatin-induced ototoxicity in mouse cochlear cultures .
    KL1333 hydrochloride

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